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Reactive oxygen species mediate oridonin-induced apoptosis through DNA damage response and activation of JNK pathway in diffuse large B cell lymphoma.
- Source :
-
Leukemia & Lymphoma . Apr2016, Vol. 57 Issue 4, p888-898. 11p. - Publication Year :
- 2016
-
Abstract
- This study investigated the cytotoxic effect of oridonin (ORI), a diterpenoid isolated fromRabdosia rubescens, in human diffuse large B cell lymphoma (DLBCL)in vitroandin vivoand the potential molecular mechanisms for ORI-induced cell apoptosis. ORI treatment caused reactive oxygen species (ROS)-mediated oxidative DNA damage response (DDR) and the c-Jun N-terminal kinase (JNK) pathway activation, leading to an induction of intrinsic apoptosis. ROS abolition blocked ORI-induced apoptosis and attenuated the expression of phospho-histone H2AX and phospho-JNK, indicating that ROS-mediated DNA damage and JNK pathway activation were involved in ORI-induced apoptosis. The systemic administration of ORI suppressed the growth of human DLBCL xenografts without showing significant toxicity. These findings suggest that ORI may have promising therapeutic application in DLBCL. [ABSTRACT FROM AUTHOR]
Details
- Language :
- English
- ISSN :
- 10428194
- Volume :
- 57
- Issue :
- 4
- Database :
- Academic Search Index
- Journal :
- Leukemia & Lymphoma
- Publication Type :
- Academic Journal
- Accession number :
- 113944749
- Full Text :
- https://doi.org/10.3109/10428194.2015.1061127